The pathogenesis of contrast-induced nephropathy is uncertain. There are two main theories. According to the first one a possible influence on renal hemodynamics, mainly vasoconstriction, resulting in medullary ischemia possibly mediated by an alteration in endothelin and adenosine. In addition to direct vasoconstriction of renal vessels, iodinated contrast agents also block an important pathway for vasodilation and autoregulation possibly by reducing the production of nitric oxide. And according to the other main theory contrast agents exert direct toxic effects on tubular epithelial cells. It seems that reactive oxygen species have a role in CIN.